Phat32 said:

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The worst remaining holdover from this whole thing.

Still waiting on data showing that airline flights are super-spreader events.

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bigtruckguy3500 said:

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Phat32 said:

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The worst remaining holdover from this whole thing.

Still waiting on data showing that airline flights are super-spreader events.

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Very difficult data to collect.

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bigtruckguy3500 said:

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Phat32 said:

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The worst remaining holdover from this whole thing.

Still waiting on data showing that airline flights are super-spreader events.

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Very difficult data to collect.

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NASAg03 said:

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bigtruckguy3500 said:

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Phat32 said:

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The worst remaining holdover from this whole thing.

Still waiting on data showing that airline flights are super-spreader events.

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Very difficult data to collect.

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They track every person on a flight and where they are seated. They could easily crunch the data.

The question is why they haven't.

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bigtruckguy3500 said:

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NASAg03 said:

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bigtruckguy3500 said:

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Phat32 said:

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The worst remaining holdover from this whole thing.

Still waiting on data showing that airline flights are super-spreader events.

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Very difficult data to collect.

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They track every person on a flight and where they are seated. They could easily crunch the data.

The question is why they haven't.

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So, sounds easy, but it really isn't. Incubation period for this is 2-14 days, with an average of 4-5 days. People travel from all over, pass through airports, sit next to other people in the terminals, travel to the airport via Uber/cab/shuttle bus, spend the night at hotels, etc.

Someone gets COVID 6 days after getting off a flight, does that mean he got it on the flight and he's showing symptoms past the average incubation period? Or did he get it after getting off the flight? Does the airline call the individual for 14 days after the flight to track if he develops symptoms? Is it up to the individual to notify the airlines that he tested positive after the flight? Did he actually develop symptoms before flying and was just hiding it so he could get home?

These are just some of the variables I came up with in about 2 minutes. I'm sure there are a lot more.

Again, this is hard data to collect, and even harder to prove causality.

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To put it simply, the "second wave" of an epidemic is not a consequence of human sin regarding mask wearing and hand shaking. Rather, the "second wave" is an inescapable consequence of an air-dryness-driven many-fold increase in disease contagiousness, in a
population that has not yet attained immunity.

If my view of the mechanism is correct (i.e., "physical loss"), then Shaman's work further necessarily implies that the dryness-driven high transmissibility (large R0) arises from small aerosol particles fluidly suspended in the air; as opposed to large droplets that are quickly
gravitationally removed from the air.

Such small aerosol particles fluidly suspended in air, of biological origin, are of every variety and are everywhere, including down to virion-sizes (Despres, 2012). It is not entirely unlikely that viruses can thereby be physically transported over inter-continental distances (e.g., Hammond, 1989).

More to the point, indoor airborne virus concentrations have been shown to exist (in day-care facilities, health centres, and onboard airplanes) primarily as aerosol particles of diameters smaller than 2.5 m, such as in the work of Yang et al. (2011):

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"Half of the 16 samples were positive, and their total virus concentrations ranged from 5800 to 37 000 genome copies m3. On average, 64 per cent of the viral genome copies were associated with fine particles smaller than 2.5 m, which can remain suspended for hours. Modelling of virus concentrations indoors suggested a source strength of 1.6 1.2 105 genome copies m3 air h1 and a deposition flux onto surfaces of 13 7 genome copies m2 h1 by Brownian motion.

Over 1 hour, the inhalation dose was estimated to be 30 18 median tissue culture infectious dose (TCID50), adequate to induce infection. These results provide quantitative support for the idea that the aerosol route could be an important mode of influenza transmission."

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Such small particles (< 2.5 m) are part of air fluidity, are not subject to gravitational sedimentation, and would not be stopped by long-range inertial impact. This means that the slightest (even momentary) facial misfit of a mask or respirator renders the design filtration norm of the mask or respirator entirely irrelevant. In any case, the filtration material itself of N95 (average pore size ~0.30.5 m) does not block virion penetration, not to mention surgical masks.

For example, see Balazy et al. (2006). Mask stoppage efficiency and host inhalation are only half of the equation, however, because the minimal infective dose (MID) must also be considered. For example, if a large number of pathogen-laden particles must be delivered to the lung within a certain time for the illness to take hold, then partial blocking by any mask or cloth can be enough to make a significant difference.

On the other hand, if the MID is amply surpassed by the virions carried in a single aerosol particle able to evade mask-capture, then the mask is of no practical utility, which is the case. Yezli and Otter (2011), in their review of the MID, point out relevant features:
most respiratory viruses are as infective in humans as in tissue culture having optimal laboratory susceptibility
it is believed that a single virion can be enough to induce illness in the host
the 50%-probability MID ("TCID50") has variably been found to be in the range 1001000
virions
there are typically 103107 virions per aerolized influenza droplet with diameter 1 m 10 m
the 50%-probability MID easily fits into a single (one) aerolized droplet
For further background:
A classic description of dose-response assessment is provided by Haas (1993).
Zwart et al. (2009) provided the first laboratory proof, in a virus-insect system, that the
action of a single virion can be sufficient to cause disease.
Baccam et al. (2006) calculated from empirical data that, with influenza A in humans,
"we estimate that after a delay of ~6 h, infected cells begin producing influenza virus
and continue to do so for ~5 h. The average lifetime of infected cells is ~11 h, and the
half-life of free infectious virus is ~3 h. We calculated the [in-body] basic reproductive
number, R0, which indicated that a single infected cell could produce ~22 new
productive infections."
Brooke et al. (2013) showed that, contrary to prior modeling assumptions, although not
all influenza-A-infected cells in the human body produce infectious progeny (virions),
nonetheless, 90% of infected cell are significantly impacted, rather than simply surviving
unharmed.

All of this to say that: if anything gets through (and it always does, irrespective of the mask), then you are going to be infected. Masks cannot possibly work. It is not surprising, therefore, that no bias-free study has ever found a benefit from wearing a mask or respirator in this application.

Therefore, the studies that show partial stopping power of masks, or that show that masks can capture many large droplets produced by a sneezing or coughing mask-wearer, in light of the above-described features of the problem, are irrelevant. For example, such studies as these:
Leung (2020), Davies (2013), Lai (2012), and Sande (2008).

Why There Can Never Be an Empirical Test of a Nation-Wide Mask-Wearing Policy

As mentioned above, no study exists that shows a benefit from a broad policy to wear masks in public. There is good reason for this. It would be impossible to obtain unambiguous and biasfree results:
Any benefit from mask-wearing would have to be a small effect, since undetected in controlled experiments, which would be swamped by the larger effects, notably the large effect from changing atmospheric humidity.
Mask compliance and mask adjustment habits would be unknown.
Mask-wearing is associated (correlated) with several other health behaviours; see Wada (2012).
The results would not be transferable, because of differing cultural habits.
Compliance is achieved by fear, and individuals can habituate to fear-based propaganda, and can have disparate basic responses.
Monitoring and compliance measurement are near-impossible, and subject to large errors.
Self-reporting (such as in surveys) is notoriously biased, because individuals have the self-interested belief that their efforts are useful.
Progression of the epidemic is not verified with reliable tests on large population samples, and generally relies on non-representative hospital visits or admissions.

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Many potential harms may arise from broad public policies to wear masks, and the following unanswered questions arise:

Do used and loaded masks become sources of enhanced transmission, for the wearer and others?
Do masks become collectors and retainers of pathogens that the mask wearer would
otherwise avoid when breathing without a mask?
Are large droplets captured by a mask atomized or aerolized into breathable components? Can virions escape an evaporating droplet stuck to a mask fiber?
What are the dangers of bacterial growth on a used and loaded mask?
How do pathogen-laden droplets interact with environmental dust and aerosols captured on the mask?
What are long-term health effects on HCW, such as headaches, arising from impeded breathing?
Are there negative social consequences to a masked society?
Are there negative psychological consequences to wearing a mask, as a fear-based behavioural modification?
What are the environmental consequences of mask manufacturing and disposal?
Do the masks shed fibres or substances that are harmful when inhaled?

Conclusion

By making mask-wearing recommendations and policies for the general public, or by expressly condoning the practice, governments have both ignored the scientific evidence and done the opposite of following the precautionary principle.

In an absence of knowledge, governments should not make policies that have a hypothetical potential to cause harm. The government has an onus barrier before it instigates a broad socialengineering intervention, or allows corporations to exploit fear-based sentiments.

Furthermore, individuals should know that there is no known benefit arising from wearing a mask in a viral respiratory illness epidemic, and that scientific studies have shown that any benefit must be residually small, compared to other and determinative factors. Otherwise, what is the point of publicly funded science?

The present paper about masks illustrates the degree to which governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum, or select only incomplete science that serves their interests. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.

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